In the study by Sabit et al,1 subjects in the group with hypoxia experienced a hypoxic challenge with a mean oxygen saturation decline from 94% ± 2% to 90% ± 3%. When the oxygen concentration in the arterial blood fell, the chemoreceptors were stimulated and the ventilation increased, as shown by a rising respiratory rate (RR) or tidal volume.8 The muscle must be loaded with additional respiratory work, possibly contributing to a surge of IL-6. Although ventilation was not measured, the findings of higher RR and heart rate (HR) in the subjects receiving the hypoxic challenge were also in part compatible with our concern. (In the group with hypoxia, the RR increased from 14 ± 1 per min to 16 ± 3 per min, and the HR increased from 86 ± 6 per min to 94 ± 4 per min; in the control group, the RR increased from 14 ± 1 per min to 15 ± 1 per min, and the HR increased from 82 ± 4 per min to 87 ± 6 per min). In this study, the role of muscle-derived IL-6 should be further clarified in order to accurately document the effect of hypoxia on IL-6.